Two Susceptibility Loci Identified for Prostate Cancer Aggressiveness

 
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Berndt, Sonja I.
Wang, Zhaoming
Yeager, Meredith
Alavanja, Michael C.
Albanes, Demetrius
Amundadottir, Laufey
Andriole, Gerald
Freeman, Laura Beane
Campa, Daniele
Cancel-Tassin, Geraldine
Canzian, Federico
Cornu, Jean-Nicolas
Cussenot, Olivier
Diver, W. Ryan
Gapstur, Susan M.
Grönberg, Henrik
Haiman, Christopher A.
Henderson, Brian
Hutchinson, Amy
Key, Timothy J.
Kolb, Suzanne
Koutros, Stella
Le Marchand, Loic
Lindström, Sara
Machiela, Mitchell J.
Ostrander, Elaine A.
Riboli, Elio
Schumacher, Fred
Siddiq, Afshan
Stanford, Janet L.
Stevens, Victoria L.
Travis, Ruth C.
Tsilidis, Konstantinos K.
Virtamo, Jarmo
Weinstein, Stephanie
Wilkund, Fredrik
Xu, Jianfeng
Zheng, S. Lilly
Yu, Kai
Wheeler, William
Zhang, Han
Sampson, Joshua
Black, Amanda
Jacobs, Kevin
Hoover, Robert N
Tucker, Margaret
Chanock, Stephen J.
Note: Order does not necessarily reflect citation order of authors.
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https://doi.org/10.1038/ncomms7889
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Berndt, S. I., Z. Wang, M. Yeager, M. C. Alavanja, D. Albanes, L. Amundadottir, G. Andriole, et al. 2015. “Two Susceptibility Loci Identified for Prostate Cancer Aggressiveness.” Nature communications 6 (1): 6889. doi:10.1038/ncomms7889. http://dx.doi.org/10.1038/ncomms7889.
Abstract
Most men diagnosed with prostate cancer will experience indolent disease; hence discovering genetic variants that distinguish aggressive from non-aggressive prostate cancer is of critical clinical importance for disease prevention and treatment. In a multistage, case-only genome-wide association study of 12,518 prostate cancer cases, we identify two loci associated with Gleason score, a pathological measure of disease aggressiveness: rs35148638 at 5q14.3 (RASA1, P=6.49×10-9) and rs78943174 at 3q26.31 (NAALADL2, P=4.18×10-8). In a stratified case-control analysis, the SNP at 5q14.3 appears specific for aggressive prostate cancer (P=8.85×10-5) with no association for non-aggressive prostate cancer compared to controls (P=0.57). The proximity of these loci to genes involved in vascular disease suggests potential biological mechanisms worthy of further investigation.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4422072/pdf/
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